IC14 PR3151 SSTI Flashcards
(Relate the anatomical site to the type of SSTI)
Epidermis
Impetigo
(Relate the anatomical site to the type of SSTI)
Dermis
Ecthyma, erysipelas
(Relate the anatomical site to the type of SSTI)
Hair follicles
Furuncles
Carbuncles (cluster of furuncles)
(Relate the anatomical site to the type of SSTI)
SubQ fat
Cellulitis
(Relate the anatomical site to the type of SSTI)
Fascia (surrounds blood vessels)
Necrotizing fasciitis
(Relate the anatomical site to the type of SSTI)
Muscle
Myositis
(Relate the anatomical site to the type of SSTI)
Skeletal muscle
Pyomyositis (purulent infection of skeletal muscle, often with abscess formation
Factors that impair skin barrier function (x9)
age (very young and old)
infection
phy dmg (pressure, friction, lacerations)
phy environment (contact w urine faeces sweat and chronic wound fluid)
ischaemia (lack of perfusion)
diseases (diabetes, etc)
drugs (immunosupps, SGLT2i, etc)
pH (unbalanced detergents, phy envi)
excess soap and detergent use
What are the protective mechanisms of the skin against SSTIs?
1) normal skin function acts as a protective barrier against infections.
2) continuous renewal of epidermal layer results in shedding of keratocytes and skin microbiota
3) sebaceous secretions inhibit growth of many bact and fungi
4) normal commensal skin microbiome prevents colonisation and overgrowth of more pathogenic strains.
5) others: pH (acidic environment of the skin), AMP anti-microbial peptides
What are the three risk factors for SSTIs?
1) disruption of the skin barrier
2) conditions that predispose to infection
3) history of cellulitis
how does a disruption of skin barrier become a risk factor for SSTI?
describe some of the conditions for the above^
- traumatic
- non-traumatic: ulcer, tinea pedis, dermatitis, toe web intertrigo, chemical irritants.
- impaired venous and lymphatic drainage (poor flow preventing rescue agents from flowing there and fight invaders + retention and overgrowth of organism causing it to invade): saphenous venectomy, obesity, chronic venous insufficiency.
- peripheral artery disease
what are the conditions (and drugs)that predispose to infection of sstis (risk factor)
- diabetes, cirrhosis, neutropenia, hiv, transplantation and immunosuppressive meds
methods to prevent SSTIs?
1) good care to maintain skin integrity: good wound care, tx of tinea pedis, preventing dry cracked skin, good foot care for DM patients to prevent wounds and ulcers.
2) identify any predisposing factors and treat at same time of initial diagnosis to reduce risk for recurrence.
3) acute traumatic wounds irrigated, foreign objects removed, devitalised tissues debrided (source control).
what history taking should be done before diagnosis of SSTI?
underlying diseases
recent trauma, bites, burns, water exposure
animal exposure
travel history
HOW should culture sample be collected for SSTIs?
1) deep in the wound after cleansing surface
2) base of a closed abscess, where bact grow, rather than surface
3) curettage (debride top) instead of wound swab or irrigation
when to collect blood culture for ssti?
when there are marked systemic symptoms of infection or the patient is immunocompromised
when and what culture samples should not be collected for sstis?
mild and superfiical infections where the skin commensal bact may be taken instead
wound swabs because it may be difficult to obtain representative sample.
what is the clinical presentation of impetigo?
begins as erythematous papules that rapidly evolve into vesicles and pustules that rupture, with the dried discharge forming honey-colored crusts on an erythematous base.
Usually on exposed areas of body (face and extremities).
Lesions well localised, frequently
many, bullous or non bullous in appearance.
what is the clinical presentation of ecthyma?
ulcerative form of impetigo in which the lesions extend through the epidermis and deep into the dermis.
Pruritis is common, scratching may further spread
infection
what is the clinical presentation of furuncle?
an infection of the hair follicle in
which purulent material extends through the dermis into
the subcutaneous tissue, where a small abscess forms
what is the clinical presentation of carbuncle?
formed when furuncles coalesce and extent
into subcutaneous tissues.
what is the clinical presentation of skin abscess?
collections of pus within the dermis and
deeper skin tissues. Skin abscesses manifest as painful, tender, fluctuant and erythematous nodules
what is the clinical presentation of erysipelas?
affects upper dermis; Fiery red, tender,painful plaque (raised above surrounding skin) with well‐demarcated edges.
Common on face, also lower extremities.
what is the clinical presentation of cellulitis ?
Involves deeper and subcutaneous fats.
Usually presents as an acute, diffuse, spreading, nonelevated, poorly demarcated area of erythema.
Relatively rapid onset/progression.
Almost always unilateral.
Fever in 20–70% of patients.
It is typically found on the lower extremities, although it can appear on any area of the skin.
what are the complications of cellulitis and erysipelas
BET LONG
Bacteremia, Endocarditis, Toxic shock, Lymphedema, Osteomyelitis,
Necrotizing soft‐tissue infections, Glomerulonephritis
what are some cellulitis mimickers and how to manage?
deep venous thrombosis, calciphylaxis, stasis dermatitis, hematoma, erythema migrans, cellulitis
just give a short course of narrow spectrum gram + and see whether patient improves. if no, explore further causes.
what are the likely pathogens for impetigo (non bullous)?
staphylococci and streptococci
usually beta hemolytic strep (A-C, G)
what are the likely pathogens for impetigo (bullous)?
toxin-producing strains of s.aureus
what are the likely pathogens for ecthyma?
usually grp A strep (strep pyrogenes)
what are the likely pathogens for non-purulent SSTI (cellulitis and erysipelas)?
mainly beta haemolytic strep (grp A-C,G), but usually grp A (strep pyrogenes)
S.aureus possible but less frequent.
Others (not common): aeromonas, vibrio vulnificus, and pseudomonas with (water exposure).
what are the likely pathogens for purulent SSTI (furuncles, carbuncles, skin abscess, purulent cellulitis)?
mainly s.aureus
sometimes beta haem strep (A-C,G)
what are some pathogenic characteristics of skin abscesses involving the peri oral, perirectal, vulvovaginal areas?
common to see isolation of multiple organisms including gram (-) and anaerobes.
CA-MRSA epidemiology?
Not common in SG, common in the US.
CA-MRSA virulence profile?
Presence of
- panton valentine leucocidin (PVL)
- SCCmecIV or staphylococcal chromosomal casette.
What are some risk factors for CA-MRSA?
contact sports, military personnel, IV drug abusers, prison inmates
overcrowded facilities, close contact and lack of sanitation.
What is the susceptibility of CA-MRSA?
what drug works against CAMRSA
oral non-beta lactams
- clindamycin
- cotrimox
- doxycycline
what is the definition of HA-MRSA?
this is an mrsa infection that occurs
> 48h following hospitalisation
OR
outside of the hospital within 12 months of exposure to healthcare
how does HA-MRSA spread in the healthcare setting?
MRSA able to form biofilm on devices
What are the risk factors of HA-MRSA
abx use, recent hosp or surgery, prolonged hosp, intensive care, hemodialysis,
proximity to others with MRSA colonisation or infectoin
what abx to use for the treatment of impetigo (mild, limited lesions)?
topical mupirocin BD x 5days
what is the efficacy of mupirocin to pathogens (gram positive cocci vs enterococci vs gram neg vs MRSA)
highly effective against gram postive cocci esp s.aureus
useful for erradication of nasal staphyloccal carriage
not effective vs enterococci and gram negs
MRSA resistance a concern
(culture directed) (MSSA))
what abx to use for the treatment of impetigo and ecthyma (multiple lesions)?
PO cephexin or cloxacillin x 7days
(empiric tx)
what abx to use for the treatment of impetigo and ecthyma (multiple lesions)?
include length of treatment
NO penicillin allergy:
- PO Ceph or cloxacillin x 7days
penicillin allergy:
- PO clindamycin x 7days
(culture directed) (s pyrogenes)
what abx to use for the treatment of impetigo and ecthyma (multiple lesions)?
include length of treatment
PO penicillin V or amoxicillin x 7days
what is the mainstay of treatment for purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
incision and drainage (I&D)
when do you use adjunctive systemic abx for purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
when
- unable to drain completely
- lack of response to I & D
- extensive disease involving several sites
- extremes of age
- immune suppressed
- signs of systemic illness (SIRS ≥2 pts)
What is the SIRS criteria for purulent SSTI
Temperature >38 or <36
HR >90
RR > 34
WBC > 12x10^9 or <4x10^9
what is the (empiric) general treatment for mild infection of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
I and D or warm compress
what is the (empiric) general treatment for moderate infection (w systemic symptoms) of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
I&D plus oral abx
- PO cloxacillin, cephalexin
OR
- PO clindamycin (penicillin allergy)
what is the severity classification for purulent SSTIs?
mild = no systemic infection
moderate - severe = systemic symptoms (classification with the SIRS scale, ≥2 points qualifies) and other risk factors (recall)
what is the (empiric) general treatment for severe infection of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
I&D plus IV abx
- IV cloxacillin or cefazolin or clindamycin or vancomycin
what is the (empiric) (MRSA) treatment of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
IF GOT MRSA RISK FACTORS
include length of treatment
mild
PO cotrimox, doxy, clindamycin x5-10 days
mod-severe
IV Vanco, dapto, linezolid
reserve dapto and linezolid is VRE or allergy
what is the (empiric) (including gram neg anaerobic) treatment of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
Recall AND state when you treat for gram neg and anaerobe
(simple)
PO amoxiclav x5-10 days
- recall that this is better for skin abscess near the perioral, perirectal, vulvovaginal…
(long hospital stay and high resistance risk)
Recall AND state when you treat for gram neg and anaerobe
SEVERE PURULENT SSTI
piptazo
what is the (empiric) (including gram neg anaerobic) treatment of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
Recall AND state when you treat for gram neg and anaerobe
(very sick, i.e., severe illness)
carbapenem
to cover for ESBL, amp c producing
what is the (empiric) treatment of mild, non-purulent SSTIs (cellulitis, erysipelas)?
i.e., no systemic signs of infection
ORAL abx
penicillin V, cephalexin, cloxacillin
x5-10days
penicillin allergy
clindamycin
x5-10days
what is the (empiric) treatment of moderate, non-purulent SSTIs (cellulitis, erysipelas)?
i.e., systemic signs with some purulence
consider additional….
IV abx
cefazolin, cloxacillin x5-10days
penicillin allergy
clindamycin x5-10days
add cipro if water exposure
when there is moderate non purulent SSTI with water exposure,
what are the extra organisms to cover for and what abx to add on for empiric tx?
vibrio, aeromonas, pseudomonas x5-10days
include ciprofloxacin
what is the (empiric) treatment of severe, non-purulent SSTIs (cellulitis, erysipelas)?
include additional therapy for MRSA risk factor coverage
add reason for change in reigmen
IV antibiotics: piptazo, cefepime, merepenem x5-10days (increase to 14 immunocompromised)
add vancomycin, daptomycin, linezolid if MRSA risk factor.
to broaden coverage and include risk for necrotizing infections
what are the signs/factors for severe non purulent sstis?
systemic signs of infection, failed oral therapy, immunocompromised.
what are the non-phx measrues for nonpurulent SSTI?
rest and limb elevation (drainage of edema and inflammatory substances)
Treat underlying conditions eg tinea pedis, skin dryness, limb edema
what are the goal and monitoring parameters for ssti?
1) resolution of s/sx
- improvement 48-72h
- no progression of lesion or development of complication
- switch to oral once better
- if no response 2-3 days, reassess condition + choice of abx
2) no need for repeat bact culture.
3) no ADR.
define DFIs in words
soft tissue or bone infections below the malleolus usually involving bacterial colonization of ulcers and wounds
what are the complications of DFIs?
hospitalisation
osteomyelitis
eventual amputation
what is the pathophysiology of DFIs?
1) Neuropathy
Peripheral: ↓ pain
sensation and altered
pain response
* Motor:muscle imbalance
* Autonomic: ↑ dryness,
cracks and fissures
2) Vasculopathy
* Early atherosclerosis
* Peripheral vascular
* disease
* Worsened by
hyperglycemia and
hyperlipidemia
3) Immunopathy
* Impaired immune
response
* ↑ susceptibility to
infections
* Worsened by
* hyperglycemia
what is the criteria for DFI?
purulent discharge
OR
≥2 s/sx of inflammation:
erythema, warm, tenderness, pain, induration
what is the clinical presentation and progression of DFIs?
Superficial ulcer,
mild erythema –> Deep tissue infection, extensive erythema –> Infection of bone and fascia, purulent discharge –> Localized gangrene
what is the evolution of DFIs?
erythema (day 1), blisters (day 3), a necrotizing abscess (day 6), and
wound infection requiring surgery (day 10).
what are the causative organisms for DFIs?
include gram positive, gram negative, and anaerobes
usually polymicrobial
gram positive most common: S.aureus and strep spp
gram negative: EKP
Pseudomonas less common
anaerobes: peptostreptococcous, veillonella, bacteriodes
when would there be presence of gram negs in DFIs?
chronic wounds/wounds treated with abx
when would there be presence of anaerobes in DFIs?
ischaemic or necrotic wounds
cultures for DFIs? when and how? consider the different classifications
Mild DFIs
* Optional
Moderate – severe DFIs
* Deep tissue cultures after cleansing and before starting antibiotics (if possible)
* Avoid skin swabs
Do not culture uninfected wounds
what are pseudomonal risk factors for DFIs
frequent water exposure, warm climate
when to cover for psuedomonas in DFIs?
risk factors
severe infection
or
mod infection with risk factors?
what is the classification for MODERATE DFI?
Infection of deeper tissue (e.g. bone, joints); or
If erythema: > 2 cm around ulcer
No signs of systemic infection
what is the classification for MILD DFI?
Infection of skin and SC tissue
+
If erythema: ≤ 2 cm around ulcer
+
No signs of systemic infection
what is the classification for SEVERE DFI?
Infection of deeper tissue (e.g. bone, joints); or
If erythema: > 2 cm around ulcer
+
Sign(s) of systemic infection
what are the organisms to cover for MILD DFI?
Streptococcus spp +
S. aureus
what are the organisms to cover for MODERATE DFI?
Streptococcus spp +
S. aureus +
gram‐negatives
(±P. aeruginosa) +
anaerobes
what are the organisms to cover for SEVERE DFI?
Streptococcus spp +
S. aureus +
gram‐negatives
(include P.aeruginosa) +
anaerobes
what is the empiric tx for MILD DFI?
PO Antibiotics
* Cephalexin
* Cloxacillin
* Clindamycin
If MRSA risk factor(s), use PO:
* Co‐trimoxazole
* Clindamycin
* Doxycycline
what is the empiric tx for MODERATE DFI?
Initial IV Antibiotics
* Amoxicillin/clavulanate
* Cefazolin (more ideal because 1st and 2nd gen)/Ceftriaxone + Metronidazole
IfMRSA risk factor(s), addIV:
* Vancomycin
* Daptomycin
* Linezolid
what is the empiric tx for SEVERE DFI? (need to expand the spectrum)
Initial IV Antibiotics
* Piperacillin‐tazobactam
* Cefepime + metronidazole
* Meropenem
* Ciprofloxacin + clindamycin
IfMRSA risk factor(s), addIV:
* Vancomycin
* Daptomycin
* Linezolid
what are some adjunctive measures to DFI
1) wound care
- debridement
- offloading
- dressing that promotes wound healing and exudate removal
2) optimal glycaemic control
3) foot care
- daily inspections
- prevent wounds and ulcers
how to diagnose and confirm infection for SSTI
based on history and physical examination
generally mild and superficial infections do not require any culture
take wound culture only if it fulfills any of the three criteria
take blood culture only if systemic symptoms or patient is immunocompromised
how to differentiate the severity non-purulent SSTIs? ie mild moderate severe
mild: no systemic symptoms
moderate: systemic symptoms and some purulence
severe: systemic symptoms with PO treatment failure, immunocompromised/suppressed
what are the addional pathogens to cover for the different severities of non-purulent SSTIs?
moderate: include MSSA coverage.
severe: broader coverage and explore possibility of necrotising infections
what are the 4 synergistic factors to pressure ulcers
friction
shearing
pressure
moisture
what are the risk factors for pressure ulcers
Reduced mobility – E.g. spinal cord injuries, paraplegic
Debilitated by severe chronic diseases – E.g. multiple sclerosis, stroke, cancer
Reduced consciousness
Sensory and autonomic impairment
– Incontinence
Extremes of age
Malnutrition
what is the criteria for pressure ulcer infection
1) purulent discharge
OR
2) ≥2 of the following:
- erythema
- tenderness
- pain
- induration
- warmth
what is the clincal presentation of pressure ulcer (4 stages)
stage 1:
- epidermis abrasion
- irregular area of tissue swelling
- no open wound
stage 2:
- dermis
- open wound
stage 3:
- subQ
- open sore or ulcer
stage 4:
- deeper tissue (joints, muscle, bone)
- deep sore or ulcer
what are the pathogens for pressure ulcer
similar to DFI
polymicrobial
how to culture for pressure ulcers
deep tissue culture or biopsy specimens
avoid skin swabs
adjunctive measures for pressure ulcers?
1) debridement of necrotic/infected tissue
2) local wound care
- normal saline preferred
- avoid harsh chemicals
3) relief of pressure
- turn/reposition every 2h
what is the dosing for daptomycin
4-6mg/kg q24
what is the dosing for linezolid
600mg q12
how to classify the severity of non-purulent SSTIs?
mild: no systemic symptoms
moderate: systemic symptoms with some purulence of the wound
severe: systemic symptoms with failed oral treatment or immunocompromised/suppressed.
what is the reason for changing the drug regimen for severe (nonpurulent) SSTI?
broaden the spectrum of activity
+
potentially cover for necrotising infections (typically anaerobic bacteria)
